海南地区人群动脉硬化性脑梗死与PCK1启动子-232基因多态性的相关性研究
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摘要
目的:探讨海南地区人群动脉硬化性脑梗死与磷酸烯醇式丙酮酸羧激酶基因(PCK1)启动子-232基因多态性的关系。方法:选取动脉硬化性脑梗死患者160例为观察组,另选取同期在我院行健康体检的成年人160例为对照组,采用聚合酶链反应-限制性片段长度多态性方法检测PCK1启动子-232基因多态性,采用超声多普勒技术检查颈总动脉内膜中层厚度和颈动脉斑块情况,并监测血糖和血脂情况。结果:观察组中GC基因型和GG基因型患者的餐后2 h血糖和LDL高于CC基因型(F=12.811,54.169,均P<0.001)。与对照组相比,观察组中GC和GG基因型频率及G等位基因频率明显较高(χ~2=13.341、10.807,均P=0.001)。在易损斑块中,观察组GC基因型和GG基因型及G等位基因的分布明显大于非易损斑块(χ~2=5.186、7.276,P=0.023、0.007)。2组不同基因型之间两侧颈总动脉内膜中层厚度比较差异无统计学意义(F=0.742、0.485、1.139、0.727,P=0.478、0.617、0.325、0.487)。结论:PCK1启动子-232基因多态性与海南地区人群动脉硬化性脑梗死的发生情况有一定相关性,其中以G等位基因较为突出。
Objective: To explore the relationship between atherosclerotic cerebral infarction and polymorphism of the phosphoenolpyruvate carboxykinase gene(PCK1) promoter-232 in the Hainan population. Methods: We recruited 160 patients with atherosclerotic cerebral infarction as the observation group and another 160 healthy adults who received check-ups during the same time as the control group. PCK1 promoter-232 gene polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP);the carotid intima-media thickness and carotid artery plaque(CAP) were detected by carotid doppler ultrasonography. The blood glucose and plasma lipids were measured. Results: The 2 h postprandial blood glucose and LDL cholesterol levels of the GC and GG genotypes in the observation group were higher than those of the CC genotype(F=12.811, 54.169, both P<0.001). Compared with that of the control group, the frequencies of GC and GG genotypes and the G allele in the observation group were significantly higher( χ~2=13.341, 10.807, all P=0.001). With vulnerable plaques, the distribution of GC and GG genotypes and the G allele in the observation group were significantly larger than that with non-vulnerable plaques(χ~2=5.186, 7.276, P=0.023, 0.007). The carotid intima-media thickness of the left and right carotid artery of different genotypes in the two groups were compared and showed no statistical difference(F=0.742, 0.485, 1.139, 0.727, P=0.478, 0.617, 0.325, 0.487).Conclusion: There is a certain connection between PCK1 promoter-232 gene polymorphism and the occurrence of atherosclerotic cerebral infarction in the population of Hainan, and the role of G allele is more prominent.
Objective: To explore the relationship between atherosclerotic cerebral infarction and polymorphism of the phosphoenolpyruvate carboxykinase gene(PCK1) promoter-232 in the Hainan population. Methods: We recruited 160 patients with atherosclerotic cerebral infarction as the observation group and another 160 healthy adults who received check-ups during the same time as the control group. PCK1 promoter-232 gene polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP);the carotid intima-media thickness and carotid artery plaque(CAP) were detected by carotid doppler ultrasonography. The blood glucose and plasma lipids were measured. Results: The 2 h postprandial blood glucose and LDL cholesterol levels of the GC and GG genotypes in the observation group were higher than those of the CC genotype(F=12.811, 54.169, both P<0.001). Compared with that of the control group, the frequencies of GC and GG genotypes and the G allele in the observation group were significantly higher( χ~2=13.341, 10.807, all P=0.001). With vulnerable plaques, the distribution of GC and GG genotypes and the G allele in the observation group were significantly larger than that with non-vulnerable plaques(χ~2=5.186, 7.276, P=0.023, 0.007). The carotid intima-media thickness of the left and right carotid artery of different genotypes in the two groups were compared and showed no statistical difference(F=0.742, 0.485, 1.139, 0.727, P=0.478, 0.617, 0.325, 0.487).Conclusion: There is a certain connection between PCK1 promoter-232 gene polymorphism and the occurrence of atherosclerotic cerebral infarction in the population of Hainan, and the role of G allele is more prominent.
引文
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[13] Pandi G, Nakka VP, Dharap A, et al. MicroRNA miR-29c down-regulation leading to de-repression of its target DNA methyltransferase 3a promotes ischemic brain damage[J]. PLoS One, 2013, 8:e58039.
[14]李凤,陈明,喻明,等. MMP-2基因多态性与动脉粥样硬化性脑梗死初发及复发相关性研究[J].中风与神经疾病杂志, 2015, 32:104-107.
[15] Pulliam JV, Xu Z, Ford GD, et al. Computational identification of conserved transcription factor binding sites upstream of genes induced in rat brain by transient focal ischemic stroke[J]. Brain Res, 2013, 1495:76-85.
[2] Kumar P, Misra S, Kumar A, et al. Association between Tumor Necrosis Factor-α(-238G/A and-308G/A)Gene Polymorphisms and Risk of Ischemic Stroke:A Meta-Analysis[J]. Pulse(Basel), 2016, 3:217-228.
[3]焦立影,王新,刘婷婷,等.纤维肌发育不良致自发性颈动脉夹层并脑梗死一例诊治分析[J].实用心脑肺血管病杂志, 2017, 25:102-105.
[4] Kumar P, Yadav AK, Kumar A, et al. Association between Interleukin-6(G174C and G572C)promoter gene polymorphisms and risk of ischaemic stroke:A meta-analysis[J]. Ann Neurosci, 2015, 22:61-9.
[5] Huck JH, Freyer D, B?ttcher C, et al. De novo expression of dopamine D2 receptors on microglia after stroke[J]. J Cereb Blood Flow Metab,2015, 35:1804-1811.
[6]冯兆章,张远鸿,腾录霞,等. CT血管造影检查联合ABCD2评分对短暂性脑缺血发作后早期脑梗死的预测价值研究[J].实用心脑肺血管病杂志, 2015, 23:110-112.
[7] Shahaduzzaman MD, Mehta V, Golden JE, et al. Human umbilical cord blood cells induce neuroprotective change in gene expression profile in neurons after ischemia through activation of Akt pathway[J]. Cell Transplant, 2015, 24:721-735.
[8]李鹏燕,朱雨岚.进展性腔隙性脑梗死的发病机制研究进展[J].神经损伤与功能重建, 2016, 11:429-431.
[9]李友,廖锋,崔理立,等.去整合素金属蛋白酶10基因启动子区多态性变化与腔隙性脑梗死发病风险的关系[J].山东医药, 2014, 54:4-7.
[10] Kamat PK, Kalani A, Givvimani S, et al. Hydrogen sulfide attenuates neurodegeneration and neurovascular dysfunction induced by intracerebral-administered homocysteine in mice[J]. Neuroscience, 2013,252:302-319.
[11]王皖芬,王凤,朱敏,等.基质金属蛋白酶8-799C/T基因多态性与颈动脉斑块易损性的关联分析[J].中华医学遗传学杂志, 2012, 29:60-63.
[12] Raida Z, Hundahl CA, Nyengaard JR, et al. Neuroglobin over expressing mice:expression pattern and effect on brain ischemic infarct size[J]. PLoS One, 2013, 8:e76565.
[13] Pandi G, Nakka VP, Dharap A, et al. MicroRNA miR-29c down-regulation leading to de-repression of its target DNA methyltransferase 3a promotes ischemic brain damage[J]. PLoS One, 2013, 8:e58039.
[14]李凤,陈明,喻明,等. MMP-2基因多态性与动脉粥样硬化性脑梗死初发及复发相关性研究[J].中风与神经疾病杂志, 2015, 32:104-107.
[15] Pulliam JV, Xu Z, Ford GD, et al. Computational identification of conserved transcription factor binding sites upstream of genes induced in rat brain by transient focal ischemic stroke[J]. Brain Res, 2013, 1495:76-85.